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Molecular and Cellular Biology, July 2004, p. 6117-6126, Vol. 24, No. 14
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.14.6117-6126.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Transcription Regulatory Complexes Bind the Human T-Cell Leukemia Virus 5' and 3' Long Terminal Repeats To Control Gene Expression

Isabelle Lemasson,{dagger} Nicholas J. Polakowski,{dagger} Paul J. Laybourn, and Jennifer K. Nyborg*

<[ERROR]zaff;1[ERROR]>Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, Colorado 80523-1870

Received 20 February 2004/ Returned for modification 26 March 2004/ Accepted 22 April 2004

The human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus that integrates randomly into the T-cell genome. Two long terminal repeats (LTRs) flank the integrated provirus. The upstream and downstream LTRs carry identical promoter sequences. Studies with other retroviruses suggest that the downstream promoter is silent and that RNA polymerases initiating at the upstream promoter proceed through the 3' LTR. In this study, we used the chromatin immunoprecipitation assay to compare the binding of transcription regulatory proteins at both the upstream and downstream promoters in HTLV-1-infected cell lines and adult T-cell leukemia-lymphoma cells. Unexpectedly, we detected a nearly equal distribution of activator (Tax, CREB, ATF-1, ATF-2, c-Fos, and c-Jun) and regulatory protein (CBP, p300, TAFII250, and polymerase II) binding at both the upstream and downstream promoters. Consistent with this observation, we found that the downstream promoter was transcriptionally active, suggesting that the two promoters are functionally equivalent. We also detected asymmetrical binding of histone deacetylases (HDAC-1, -2, and -3) at both promoters. All three HDACs strongly repressed Tax transactivation, and this repression correlated with displacement of Tax from the HTLV-1 promoter. These effects were reciprocal, as Tax expression reversed HDAC repression and displaced HDACs from the HTLV-1 promoter. These data suggest that HTLV-1 transcriptional regulation at both the 5' and 3' LTRs is mediated, in part, through the mutually exclusive binding of Tax and HDACs at the proviral promoters.

* Corresponding author. Mailing address: Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, CO 80523-1870. Phone: (970) 491-0420. Fax: (970) 491-0434. E-mail: Jennifer.Nyborg{at}colostate.edu.

{dagger} I.L. and N.J.P. contributed equally to this work.

Molecular and Cellular Biology, July 2004, p. 6117-6126, Vol. 24, No. 14
0022-538X/04/$08.00+0     DOI: 10.1128/MCB.24.14.6117-6126.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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